Viruses as Regulators of Delayed Hypersensitivity T-Cell and Suppressor T-Cell Function

There are a number of strategies employed by viruses to ensure their survival in a particular host or population. Nearly all such strategies involve outwitting the host’s immune defenses either directly or indirectly. Of these virus mechanisms, those that directly affect the balance between helper and suppressor T-cell responses are considered here. Viruses can potentially create this imbalance in a number of ways: For instance specific T cells can become infected, thereby compromising specific regulatory functions, or antigen-presenting cells can become infected thereby interfering with antigen presentation and consequently the induction of specific immune responses. These mechanisms may be highly relevant in the case of certain lymphotropic viruses, such as measles, or macrophage “tropic” viruses such as lactic dehydrogenase virus, both of which are also capable of persisting in their respective target cells. Despite the likely importance of such mechanisms in disturbing specific and nonspecific immune reactivity, attention here is focused on the importance of the route of entry of viruses into the host and the state of a particular virus, i.e., whether infective or not, as determining whether helper/delayed hypersensitivity T-cell or suppressor T-cell responses predominate in vivo. In particular, the importance of these T-cell subsets in protecting the host from viral disease, as well as as inducers of immune-mediated pathology is considered. However before this, a knowledge of the induction of delayed hypersensitivity (DH) and suppressor T-cell responses to viruses is presented.